Maintenance of ER homeostasis through activation of the IRE-1 and PEK-1 pathways under basal physiological conditions during development.

(A) The increase in both IRE-1 and PEK-1 activities in XBP-1 deficiency in the absence of exogenous compounds to impose ER stress, combined with the temperature-sensitive lethality of the UPR mutants, implies that UPR signaling maintains ER homeostasis not only in response to the extremes of ER stress, but also under basal physiological conditions. (B) Infection, basal growth and development, and elevated physiological temperature all contribute to ER stress, leading to lethality of UPR mutants as indicated by dashed lines.